SURGERY CASE WRITE UP

Patient’s details Patient’s name

: Nurul Hayat

Age

: 20 years old

Race

: Malay

Address

: Muar (Kampung Kelantan)

Occupation

: Student

Date of admission

: 10 March 2015

Chief complaint Abdominal pain at left iliac fossa for 1 day

History of presenting illness 1. 2. 3. 4.

5. 6. 7. 8. 9. 10. 11.

Patient had abdominal pain at left iliac fossa in the morning on 14 April 2015. The pain lasted for more than 4 hours. she came to emergency department at 4pm and got admitted to the hospital. Abdominal pain: a. Character: pricky in nature b. Onset: gradual onset c. Duration: 4-5hours d. Severity: 8-9/10 e. Aggravating factor: pain increases on movement f. Relieving factor: Rest, lay on bed g. Associated symptoms: no vomiting, no diarrhoea and no fever She having constipation problem since childhood until now. Normally her bowel movement is 2-3 days once and only once in a day. She pass stool last yesterday night. She claim that the stool is hard and dark brown in colour but no blood and mucous seen. She also experiences sensation of incomplete evacuation(tenesmus)and she was able to pass flatus She denied of having abdominal bloating, distention, loss of appetite, and loss of weight. Urination is normal which is 2-3 times per day and with no any complication.

Menstrual history 1. She attained menarche at the age of 12 years old. 2. She having regular cycle of 28-30days with duration of 3 days 3. She denied of having menorrhagia, dysmenorrhea and any previous history of gynaecological problems.

Past medical history

Unremarkable Past surgical history Unremarkable Family history 1. Parents: no medical illness 2. Siblings: Asthma( sister and brother) 3. Has history of nasopharyngeal carcinoma in the family Social history 1. She is a non-smoker and non-alcoholic 2. Diet: a. normally takes soft food like soup, and porridge b. she usually takes frequent meals which is about 5-6 times per day c. Takes less spicy food, vegetable and fruits. 3. She is not allergic to any drugs or food. 4. PROVISIONAL DIAGNOSIS Sub-acute intestinal obstruction DIFFERENTIAL DIAGNOSIS 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Mesenteric ischemia Colorectal ca Volvulus Colitis Inflammatory bowel disease Strangulated hernia Renal stone Ureteric stone Intestinal polyps Pelvic masses Ileitis Psoas abcess Diverticulitis Tuboovarian cyct Tuboovarian abcess Salphingitis

DISCUSSION INVESTIGATION IMAGING

Erect abdominal films are no longer routinely obtained and the radiological diagnosis is based on a supine abdominal filmAn erect film may subsequently be requested when further doubt exists. When distended with gas, the jejunum, ileum, caecum and remaining colon have a characteristic appearance in adults and older children that allows them to be distinguished radiologically. In intestinal obstruction, fluid levels appear later than gas shadows as it takes time for gas and fluid to separate. These are most prominent on an erect film. In adults, two inconstant fluid levels – one at the duodenal cap and the other in the terminal ileum – may be regarded as normal. In infants (less than one year old), a few fluid levels in the small bowel may be physiological. In this age group, it is difficult to distinguish large from small bowel in the presence of obstruction, because the characteristic features seen in adults are not present or are unreliable. During the obstructive process, fluid levels become more conspicuous and more numerous when paralysis has occurred. When fluid levels are pronounced, the obstruction is advanced. In the small bowel, the number of fluid levels is directly proportional to the degree of obstruction and to its site, the number increasing the more distal the lesion In patients without evidence of strangulation, there is a role for other imaging modalities. A recent systematic review and meta-analysis of the diagnostic and therapeutic role of 50–100 mL water-soluble contrast agent in adhesive small bowel obstruction included 14 prospective studies. The appearance of contrast in the colon 4–24 hours after administration had a sensitivity of 96 per cent and a specificity of 98 per cent in predicting resolution of small bowel obstruction. If contrast does not reach the colon, surgery is required in about 90 per cent of patients. Administration of a water-soluble agent was also effective in reducing the need for surgey (OR 0.62; p = 0.007) and shortening hospital stay. Radiological features of obstruction (on plainx-ray) 1. 2. 3. 4. 5. 6.

The obstructed small bowel is characterised by straight segments that are generally central and lie transversely. No/minimal gas is seen in the colon The jejunum is characterised by its valvulae conniventes, which completely pass across the width of the bowel and are regularly spaced, giving a ‘concertina’ or ladder effect Ileum – the distal ileum has been piquantly described by Wangensteen as featureless Caecum – a distended caecum is shown by a rounded gasshadow in the right iliac fossa Large bowel, except for the caecum, shows haustral folds, which, unlike valvulae conniventes, are spaced irregularly, do not cross the whole diameter of the bowel and

The CT scan is now used very widely to investigate all forms of intestinal obstruction. It is highly accurate and its only limitations are in diagnosing ischaemia. It is important to remember that even with the best imaging techniques, the diagnosis of strangulation remains a clinical one. Impacted foreign bodies may be seen on abdominal radiographs. It is noteworthy that gas-filled loops and fluid levels in the small and large bowel can also be seen in established paralytic ileus and pseudoobstruction. The former can, however, normally be distinguished on clinical grounds, whereas the latter can be confirmed radiologically. Fluid levels may also be seen in non-obstructing conditions such as gastroenteritis, acute pancreatitis and intra-abdominal sepsis.

TREATMENT OF ACUTE INTESTINAL OBSTRUCTION There are three main measures used to treat acute intestinal obstruction 1. Gastrointestinal drainage via a nasogastric tube 2. Fluid and electrolyte replacement

3. Relief of obstruction 4. Surgical treatment is necessary for most cases of intestinal obstruction but should be delayed until resuscitation is complete, provided there is no sign of strangulation or evidence of closed-loop obstruction The first two steps are always necessary before attempting the surgical relief of obstruction and are the mainstay of postoperative management. Principles of surgical intervention for obstruction Management of:   

The segment at the site of obstruction The distended proximal bowel The underlying cause of obstruction

Supportive management Nasogastric decompression is achieved by the passage of a non-vented (Ryle) or vented (Salem) tube. The tubes are normally placed on free drainage with 4-hourly aspiration, but may be placed on continuous or intermittent suction. As wellmas facilitating decompression proximal to the obstruction, they are essential to reduce the risk of subsequent aspiration during induction of anaesthesia and postextubation. The basic biochemical abnormality in intestinal obstruction is sodium and water loss, and therefore the appropriate replacement is Hartmann’s solution or normal saline. The volume required varies and should be determined by clinical haematological and biochemical criteria. Antibiotics are not mandatory but many clinicians initiate broad-spectrum antibiotics early in therapy because of bacterial overgrowth. Antibiotic therapy is mandatory for all patients undergoing surgery for intestinal obstruction. Surgical treatment The timing of surgical intervention is dependent on the clinical picture. Indications for early surgical intervention   

Obstructed external hernia Clinical features suspicious of intestinal strangulation Obstruction in a ‘virgin’ abdomen

Operative decompression should be performed whenever possible. This reduces pressure on the abdominal wound reducing pain and improving diaphragmatic movement. The simplest and safest method is to insert a large bore orogastric tube and to milk the small bowel contents in a retrograde manner to the stomach for aspiration. All volumes of fluid removed should bemaccurately measured and appropriately replaced. It is important to ensure that the stomach is empty at the end of the procedure to prevent postoperative aspiration. Rarely, decompression using Savage’s decompressor within a seromuscular purse-string suture may be required. Its benefits should be balanced against the potential risk of septic complications from spillage and the risk of leakage from the suture line postoperatively. The type of surgical procedure required will depend upon the cause of obstruction – division of adhesions (enterolysis), excision, bypass or proximal decompression. Following relief of

obstruction, the viability of the involved bowel should be carefully assessed (Table 70.3). Although frankly infarcted bowel is obvious, the viability status in many cases may be difficult to discern. If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and then reassessed. The state of the mesenteric vessels and pulsation in adjacent arcades should be sought. Viability is also confirmed by colour, sheen and peristalsis. If at the end of this period, there is still uncertainty about gut viability, the gut should be resected if this does not result in short bowel syndrome. If the patient is septic such that they require inotropic therapy or would require postoperative level 3 intensive care treatment following resection, consideration should be given to raising both ends of the bowel as stomas. This is not only safe, but also allows regular assessment of the bowel. Intestinal ischaemia/reperfusion injury has been described following reperfusion of ischaemic bowel with remote lung injury resulting from the release of inflammatory mediators. This should be borne in mind when dealing with ischaemic bowel. For example, if there is a volvulus with established infarction, detorsion should be avoided until the affected mesentery has been clamped and thus reperfusion injury prevented. When no resection has been undertaken or there are multiple ischaemic areas (mesenteric vascular occlusion), a second-required will depend upon the cause of obstruction – division of adhesions (enterolysis), excision, bypass or proximal decompression. Following relief of obstruction, the viability of the involved bowel should be carefully . Although frankly infarcted bowel is obvious, the viability status in many cases may be difficult to discern. If in doubt, the bowel should be wrapped in hot packs for 10 minutes with increased oxygenation and then reassessed. The state of the mesenteric vessels and pulsation in adjacent arcades should be sought. Viability is also confirmed by colour, sheen and peristalsis. If at the end of this period, there is still uncertainty about gut viability, the gut should be resected if this does not result in short bowel syndrome. If the patient is septic such that they require inotropic therapy or would require postoperative level 3 intensive care treatment following resection, consideration should be given to raising both ends of the bowel as stomas. This is not only safe, but also allows regular assessment of the bowel. Treatment of adhesive obstruction 1. Initially treat conservatively provided there are no signs of strangulation; should rarely continue conservative treatment for longer than 72 hours 2. At operation, divide only the causative adhesion(s) and limit dissection 3. Repair serosal tears; invaginate (or resect) areas of doubtful viability 4. Laparoscopic adhesiolysis in the hands of advanced laparoscopic practitioners Treatment of recurrent intestinal obstruction caused by adhesions Several procedures may be considered in the presence of recurrent obstruction including:     

repeat adhesiolysis (enterolysis) alone; Noble’s plication operation; Charles–Phillips transmesenteric plication Intestinal intubation.

CHRONIC LARGE BOWEL OBSTRUCTION

The symptoms of chronic intestinal obstruction may arise from two sources – the cause and the subsequent obstruction. The causes of obstruction may be organic:   

intraluminal (rare) – faecal impaction intrinsic intramural – strictures (Crohn’s disease, ischaemia, diverticular), anastomotic stenosis extrinsic intramural (rare) – metastatic deposits (ovarian), endometriosis, stomal stenosis; or functional o Hirschsprung’s disease, idiopathic megacolon, pseudoobstruction.

The symptoms of chronic obstruction differ in their predominance, timing and degree from acute obstruction. In functional cases, the symptoms may have been present for months or years. Constipation appears first. It is initially relative and then absolute, associated with distension. In the presence of large bowel disease, the point of greatest distension is in the caecum, and this is heralded by the onset of pain. Vomiting is a late feature and therefore dehydration is less severe. Examination is unremarkable, save for confirmation of distension (which can be profound) and the onset of peritonism in late cases. Rectal examination may confirm the presence of faecal impaction or a tumour. Investigation Plain abdominal radiography confirms the presence of large bowel distension. All such cases should be investigated by a subsequent single-contrast water-soluble enema study, CT scan or endoscopic assessment to rule out functional disease Principles of investigation of possible largebowel obstruction In the presence of large bowel obstruction, a single contrast water-soluble enema or CT should be undertaken to exclude a functional cause ADYNAMIC OBSTRUCTION Paralytic ileus This may be defined as a state in which there is failure of transmission of peristaltic waves secondary to neuromuscular failure (i.e. in the myenteric (Auerbach’s) and submucous (Meissner’s) plexuses). The resultant stasis leads to accumulation of fluid and gas within the bowel, with associated distension, vomiting, absence of bowel sounds and absolute constipation. Varieties The following varieties are recognised: 

 

Postoperative. A degree of ileus usually occurs after any abdominal procedure and is selflimiting, with a variable duration of 24–72 hours. Postoperative ileus may be prolonged in the presence of hypoproteinaemia or metabolic abnormality Infection. Intra-abdominal sepsis may give rise to localised or generalised ileus. Reflex ileus. This may occur following fractures of the spine or ribs, retroperitoneal haemorrhage or even the application of a plaster jacket. Metabolic. Uraemia and hypokalaemia are the most common contributory factors.

Clinical features Paralytic ileus takes on a clinical significance if, 72 hours after laparotomy:  

there has been no return of bowel sounds on auscultation; there has been no passage of flatus.

Abdominal distension becomes more marked and tympanitic. Colicky pain is not a feature. Distension increases pain from the abdominal wound. In the absence of gastric aspiration, effortless vomiting may occur. Radiologically, the abdomen shows gasfilled loops of intestine with multiple fluid levels (if an erect film is felt necessary). Management Nasogastric tubes are not required routinely after elective intraabdominal surgery. Paralytic ileus is managed with the use of nasogastric suction and restriction of oral intake until bowel sounds and the passage of flatus return. Electrolyte balance must be maintained. The use of an enhanced recovery programme with early introduction of fluids and solids is, however, becoming increasingly popular. Specific treatment is directed towards the cause, but the following general principles apply: 1. 2. 3. 4.

If a primary cause is identified, this must be treated. Gastrointestinal distension must be relieved by decompression. Close attention to fluid and electrolyte balance is essential. There is no place for the routine use of peristaltic stimulants. Rarely, in resistant cases, medical therapy with a gastroprokinetic agent, such as domperidone or erythromycin may be used, provided that an intraperitoneal cause has been excluded. 5. If paralytic ileus is prolonged, CT scanning is the effective investigation; it will demonstrate any intraabdominal sepsis or mechanical obstruction and therefore guide any requirement for laparotomy. Otherwise the decision to take a patient back to theatre in these circumstances is always difficult. The need for a laparotomy becomes increasingly likely the longer the bowel inactivity persists, particularly if it lasts for more than 7 days or if bowel activity recommences following surgery and then stops again.

Pseudo-obstruction This condition describes an obstruction, usually of the colon, that occurs in the absence of a mechanical cause or acute intraabdominal disease. It is associated with a variety of syndromes in which there is an underlying neuropathy and/or myopathy and a range of other factors

Small intestinal pseudo-obstruction This condition may be primary (i.e. idiopathic or associated with familial visceral myopathy) or secondary. The clinical picture consists of recurrent subacute obstruction. The diagnosis is made by the exclusion of a mechanical cause. Treatment consists of initial correction of any underlying disorder. Metoclopramide and erythromycin may be of use. Colonic pseudo-obstruction

This may occur in an acute or a chronic form. The former, also known as Ogilvie’s syndrome, presents as acute large bowel obstruction. Abdominal radiographs show evidence of colonic obstruction, with marked caecal distension being a common feature. Indeed, caecal perforation is a well-recognised complication. The absence of a mechanical cause requires urgent confirmation by colonoscopy or a single-contrast water-soluble barium enema or CT. Once confirmed, pseudoobstruction requires treatment of any identifiable cause. If this is ineffective, intravenous neostigmine should be given (1 mg intravenously), with a further 1 mg given intravenously within a few minutes if the first dose is ineffective. During this procedure, it is best to sit the patient on a commode. ECG monitoring is required and atropine should be available. If neostigmine is not effective, colonoscopic decompression should be performed. Caecal perforation can occur in pseudo-obstruction. Abdominal examination should pay attention to tenderness and peritonism over the caecum and as with mechanical obstruction, caecal perforation is more likely if the caecal diameter is 14 cm or greater. Surgery is associated with high morbidity and mortality and should be reserved for those with impending perforation when other treatments have failed or perforation has occurred. Rarely, an endoscopically placed tube colostomy is used as a vent for patients with those with a chronic unremitting condition.